2013
Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling
Shi Y, Gochuico BR, Yu G, Tang X, Osorio JC, Fernandez IE, Risquez CF, Patel AS, Shi Y, Wathelet MG, Goodwin AJ, Haspel JA, Ryter SW, Billings EM, Kaminski N, Morse D, Rosas IO. Syndecan-2 Exerts Antifibrotic Effects by Promoting Caveolin-1–mediated Transforming Growth Factor-β Receptor I Internalization and Inhibiting Transforming Growth Factor-β1 Signaling. American Journal Of Respiratory And Critical Care Medicine 2013, 188: 831-841. PMID: 23924348, PMCID: PMC3826270, DOI: 10.1164/rccm.201303-0434oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBleomycinBronchoalveolar LavageCaveolin 1Disease Models, AnimalGene Expression ProfilingGenetic MarkersHumansHydroxyprolineIdiopathic Pulmonary FibrosisIn Vitro TechniquesMacrophages, AlveolarMiceMice, TransgenicSignal TransductionSyndecan-2Tissue Array AnalysisTransforming Growth Factor beta1Up-RegulationConceptsHuman syndecan-2TGF-β1 target genesSyndecan-2Target genesIdiopathic pulmonary fibrosisEpithelial cell apoptosisAlveolar epithelial cellsEpithelial cellsTransforming Growth Factor-β1 SignalingCell apoptosisAntifibrotic effectsTGF-β1TGF-β signalingLung injuryPulmonary fibrosisAlveolar epithelial cell apoptosisExtracellular matrix productionTransgenic miceGrowth factor-β1 (TGF-β1) signalingMacrophage-specific overexpressionLung fibrosisMicroarray assayΒ1 signalingAlveolar macrophagesDownstream expression
2006
Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis
Wang XM, Zhang Y, Kim HP, Zhou Z, Feghali-Bostwick CA, Liu F, Ifedigbo E, Xu X, Oury TD, Kaminski N, Choi AM. Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Journal Of Experimental Medicine 2006, 203: 2895-2906. PMID: 17178917, PMCID: PMC1850940, DOI: 10.1084/jem.20061536.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBleomycinCaveolin 1Collagen Type IEpithelial CellsExtracellular MatrixFibroblastsFibronectinsFibrosisGene ExpressionHumansHydroxyprolineJNK Mitogen-Activated Protein KinasesLungMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 8PhosphorylationPulmonary FibrosisRNA, Small InterferingSmad2 ProteinTransfectionTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisCav-1 expressionCav-1Pulmonary fibroblastsPrimary pulmonary fibroblastsNovel therapeutic targetProgressive chronic disorderLung tissue samplesActivation of fibroblastsGrowth factor beta1Smad signaling cascadesHuman pulmonary fibroblastsC-Jun N-terminal kinase (JNK) pathwayIPF patientsLung fibrosisProfibrotic cytokinesChronic disordersN-terminal kinase pathwayLung tissueTherapeutic targetFibrosisHydroxyproline contentHistological analysisMarked reduction
2003
Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects
Ortiz LA, Gambelli F, McBride C, Gaupp D, Baddoo M, Kaminski N, Phinney DG. Mesenchymal stem cell engraftment in lung is enhanced in response to bleomycin exposure and ameliorates its fibrotic effects. Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 8407-8411. PMID: 12815096, PMCID: PMC166242, DOI: 10.1073/pnas.1432929100.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinBone Marrow TransplantationCollagenDrug ResistanceEnzyme InductionFemaleFibrosisGene Expression RegulationGraft SurvivalHydroxyprolineIn Situ Hybridization, FluorescenceLungMaleMatrix MetalloproteinasesMesodermMiceMice, Inbred BALB CMice, Inbred C57BLOsteopontinPolymerase Chain ReactionPulmonary FibrosisRNA, MessengerSialoglycoproteinsStem Cell TransplantationTransplantation, HeterotopicConceptsLung tissueMesenchymal stem cellsCollagen depositionResistant BALB/c miceMesenchymal stem cell engraftmentBALB/c miceTotal lung DNAControl-treated miceDonor-derived cellsWhole lung tissueStem cell engraftmentType II epithelial cellsTransplant recipientsC57BL/6 recipientsMSC administrationEpithelium-like morphologyFibrotic effectsIntracranial transplantationMSC transplantationC miceBleomycin exposureLung DNAMurine bone marrowReal-time PCRBone marrow
2002
Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans
Zuo F, Kaminski N, Eugui E, Allard J, Yakhini Z, Ben-Dor A, Lollini L, Morris D, Kim Y, DeLustro B, Sheppard D, Pardo A, Selman M, Heller RA. Gene expression analysis reveals matrilysin as a key regulator of pulmonary fibrosis in mice and humans. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 6292-6297. PMID: 11983918, PMCID: PMC122942, DOI: 10.1073/pnas.092134099.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisFibrotic lungsHuman pulmonary fibrosisPotential therapeutic targetGene expression analysisClinical diseaseSmooth muscleKnockout miceTherapeutic targetFibrosisHuman tissue samplesUntreatable groupLungTissue samplesMolecular pathwaysGlobal gene expression analysisExtracellular matrix formationMiceExpression analysisMatrilysinMolecular mechanismsKey regulatorGene expression patternsExpression patternsOligonucleotide microarrays